Physiology 101: Liver and Thyroid
Thyroid, of course, is primarily known as the hormone responsible for your metabolism—defined as the chemical processes that keep your body going. The fuel required for metabolism is primarily glucose. You can get glucose from your food, of course—but if you haven’t eaten in awhile (or you’re in the middle of intense exercise), the job of maintaining blood sugar falls to the liver. The liver produces glycogen (essentially a bunch of glucose molecules linked together), and glycogen can be quickly broken apart into glucose whenever necessary.
But in order to make glycogen, the liver needs to receive signals from the thyroid. How this happens: the pituitary produces TSH, which tells the thyroid to make T4; T4 then goes to the peripheral tissues (mostly the liver, kidneys, and muscles) and turns into the much more active T3. The signal the liver needs to produce glycogen is primarily T3. If there’s not enough T3, you’ll get less glycogen formation. Less glycogen means two things: 1) hypoglycemia (low blood sugar), and 2) poor phase 2 detoxification.
Blood Sugar and Thyroid
When your glucose is low and the liver can’t compensate, cortisol, the “stress” hormone, does it for you. But anytime your body is stressed (i.e. cortisol is elevated), it signals your body that there’s a problem—such as illness or injury, and it needs to slow down in order to take care of it. This means the T4 hormone produced by the thyroid will get converted into reverse T3 instead of T3, effectively putting the brakes on your metabolism.
Putting the brakes on metabolism also means your liver produces less glycogen… and round and round we go.
Detoxification, Estrogen, and Thyroid
The other problem with low glycogen is that glycogen is the precursor for glucuronic acid, which is required for the glucuronidation pathway of the liver’s Phase 2 Detoxification. The glucuronidation pathway detoxifies steroid hormones (like estrogen)… so when your glucuronidation pathway is backed up, you will likely end up with estrogen dominance. (Hypothyroidism can also cause estrogen dominance, because it will both lower Sex Hormone Binding Globulin, and decrease progesterone production as well.)
High estrogen and low progesterone levels also perpetuate hypothyroidism: Progesterone facilitates release of T4 from the thyroid, and so high estrogen suppresses it, and high estrogen also encourages production of Thyroid Binding Globulin. TBG will bind thyroid hormone and prevent it from stimulating the thyroid receptors, rendering it ineffective.
Finally, as mentioned above, when your thyroid isn’t working as well, it puts the brakes on producing glycogen, which encourages cortisol release. In addition to perpetuating hypothyroidism, high cortisol also encourages estrogen dominance by decreasing progesterone production (because progesterone is cortisol’s parent hormone).
Not only does high estrogen perpetuate hypothyroidism; this study shows that it may be a potential trigger for Hashimoto’s Thyroiditis.
Hypothyroidism can lower 1) liver conversion of T4 to T3, and 2) liver production of glycogen (and a backed up liver can, by the same token, cause hypothyroidism).
Lower liver production of glycogen perpetuates hypothyroidism, but also increases cortisol and estrogen dominance (which, in addition to symptoms associated with high cortisol and estrogen dominance, will also both worsen hypothyroidism.
The body consists of many feedback loops. It’s all interconnected!